Antihypertensive Drug Use and The Risk of Prostate Cancer (Canada)

Perron, Linda; Bairati, Isabelle; Harel, François; Meyer, François

doi:10.1023/b:caco.0000036152.58271.5e

Cited by 152 publications

(150 citation statements)

References 28 publications

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“…There are studies that suggest that a-blockers may have some role in the development of prostate cancer, 20,21 but there are no studies relating this polymoprhism, antihypertensive treatment, and cancer. Furthermore, the GenHAT interaction result diminished when adjusted for cigarette smoking.…”

Section: Discussionmentioning

confidence: 99%

Antihypertensive therapy, the α-adducin polymorphism, and cardiovascular disease in high-risk hypertensive persons: the Genetics of Hypertension-Associated Treatment Study

et al. 2006

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Section: Discussionmentioning

confidence: 99%

Antihypertensive therapy, the α-adducin polymorphism, and cardiovascular disease in high-risk hypertensive persons: the Genetics of Hypertension-Associated Treatment Study

et al. 2006

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“…In prostate and breast cancer cell lines, epinephrine (important in acute and chronic stress) reduced the sensitivity of cancer cells to apoptosis through interaction with ADRB2 receptors followed by protein kinase A-dependent BAD phosphorylation [60]. Although large-scale human studies are lacking, a recent epidemiological study showed a decreased incidence of prostate cancer in patients who took beta-blockers regularly thereby implying the importance of the activation of β-adrenergic receptors on the development of prostate cancer [61].…”

Section: Cell Survivalmentioning

confidence: 99%

Neuroendocrine influences on cancer biology

Thaker

Sood

2008

Seminars in Cancer Biology

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Over the past 25 years, epidemiological and clinical studies have linked psychological factors such as stress, chronic depression, and lack of social support to the incidence and progression of cancer [1,2]. Although the mechanisms underlying these observations are not completely understood, recent molecular and animal studies have begun to identify specific signaling pathways that could explain the impact of neuroendocrine effects on tumor growth and metastasis. This review will highlight the importance of known clinical, molecular, and cellular processes with regard to the neuroendocrine stress effects on tumor biology and discuss possible behavioral and pharmacological interventions to ameliorate these effects and ultimately improve cancer outcomes.

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“…74 Another study concludes that b blockers may produce a general decrease in cancer risk, 75 and a second study found a decrease in prostate cancer rate with b blocker use. 76 On the other hand, a few studies have shown that use of b blockers either has no effect on the rate of breast cancer 77,78 or may even increase it. 79 Any NE level lowering or receptor blocking drug could potentially lower rates of carcinogenesis in humans, and this hypothesis is immediately testable through epidemiological investigation of medical records of large numbers of people who have taken these drugs.…”

Section: Literature Search Detailsmentioning

confidence: 99%

“…And when examining whether NE drugs affect cancer rates, it is not only important to compare people who are taking these drugs for a condition such as hypertension with healthy control subjects (some of whom may be taking these drugs), but also with hypertensive people taking classes of drugs that do not affect the NE system. 76 If NE is indeed an etiological factor in various types of cancer through activation of its extracellular receptors, drugs that affect its level or block its receptors may have an additive or synergistic preventative effect when paired with existing cancer preventing drugs that may have independent mechanisms of action, such as tamoxifen or anastrozole. 81 In a rodent model, estradiol has been shown to interact with the NE system in a manner that is thought to contribute to carcinogenesis.…”

Section: Literature Search Detailsmentioning

confidence: 99%

Is norepinephrine an etiological factor in some types of cancer?

Fitzgerald

2008

Intl Journal of Cancer

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I examine evidence that the signaling molecule norepinephrine (NE) is an etiological factor in some types of cancer. In support of this hypothesis, I cite the following 7 lines of evidence: (i) rodent studies of tumorigenesis in the context of NE manipulation; (ii) human studies of tricyclic antidepressant use and cancer rate; (iii) existence of pheochromocytoma, a cancer of the adrenal glands; (iv) cancer rate in families with individuals who have bipolar disorder; (v) hypertension and cancer risk; (vi) excessive body weight and cancer risk; and (vii) psychological stressors and cancer risk. Three aspects of the body's NE system are consistent with it playing an etiological role in various types of cancer: (i) NE circulates in the blood and can thereby access organ systems throughout the body, in addition to direct peripheral release by the sympathetic nervous system and being released within the brain; (ii) many of the body's organs possess NE receptors on the outer surface of at least some of their cells; (iii) by binding to its extracellular receptors, NE affects intracellular second messenger systems that could influence carcinogenesis. Most importantly, use of existing pharmaceutical drugs that either lower the level of NE (such as clonidine) or block NE receptors may lower the probability of an individual developing cancer, and this hypothesis could be tested immediately by an epidemiologist through examination of existing medical records. ' 2008 Wiley-Liss, Inc.Key words: norepinephrine; pharmacology; clonidine; adrenoceptor; rodent; hypertension; epidemiology; pheochromocytoma I present evidence that the signaling molecule norepinephrine (NE), which is a neurotransmitter and plays various roles in organs other than the brain, is an etiological factor in some types of cancer. In support of this hypothesis, I cite the following 7 lines of evidence: (i) in a series of rodent studies, increasing the level of NE in various organs increases tumorigenesis, whereas decreasing the level decreases tumorigenesis; (ii) in humans, tricyclic antidepressant use, which may boost the level of NE throughout the body, may be associated with increased rates of cancer; (iii) pheochromocytoma, which is a cancer of the adrenal glands, may be an example of NE causing cancer in the organ that releases it into the bloodstream; (iv) families with individuals who have bipolar disorder have elevated cancer rates, where bipolar disorder may be associated with a high level of NE; (v) hypertension is associated with an elevated level of NE in the bloodstream, and may be a cancer risk factor; (vi) excessive body weight is associated with elevated blood NE and is a cancer risk factor; and (vii) psychological stressors are associated with increased release of NE in the brain and bloodstream, and exposure to stress is potentially a cancer risk factor.In addition to the above evidence, including NE's role in the brain, several other aspects of the body's NE system are consistent with an etiological role in cancer: (i) In addition to relea...

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Antihypertensive Drug Use and The Risk of Prostate Cancer (Canada)

Abstract: Our results suggest that BBs and long-term use of ABs may prevent PC whereas calcium channel blockers or angiotensin-converting enzyme inhibitors do not influence PC risk.

Cited by 152 publications

References 28 publications

Antihypertensive therapy, the α-adducin polymorphism, and cardiovascular disease in high-risk hypertensive persons: the Genetics of Hypertension-Associated Treatment Study

Antihypertensive therapy, the α-adducin polymorphism, and cardiovascular disease in high-risk hypertensive persons: the Genetics of Hypertension-Associated Treatment Study

Neuroendocrine influences on cancer biology

Is norepinephrine an etiological factor in some types of cancer?

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